Cytoplasmic organelle present in the plant and animal cells, the mitochondria plays a primordial role for these cells. Indeed, mitochondria are announced to be << the energetic power stations of our cells >> with the production and the storage of adenosine triphosphate (ATP), universal energetic component necessary to any eukaryote cell functioning.
The comburent, necessary for such a production via a cluster of redox chemical reactions commonly called “the mitochondrial respiratory chain”, is oxygen. Oxygen is thus essential to the cell functioning, but paradoxically, it is also the initial and parallel source of reactive species called “oxygen-derived reactive species” (ERO in French, ROS in English) which are potentially toxic for cell biochemical macromolecules (DNA, proteins, lipids, etc.).
In order to neutralize this ROS formation, any cell naturally develop some antioxidant defense systems, enzymatic or not, requiring some energy to operate, which is in the first place precisely this ATP issued from the mitochondrial respiratory chain (Singh K. K., FEMS Yeast Res., 2004, vol. 5, pp. 127-132). But when an imbalance between ROS production and removal by intracellular defense systems emerges as ROS amounts become too intense, the resulting oxidant stress thus generates gradually a decline of mitochondrial functions, notably expressed by a disruption of the energy-producer electrons' flux and by a ROS formation within the mitochondria, called “intra-mitochondrial ROS” (Jones D. P., Chemico Biological Comm., 2006, vol. 163, pp. 38-53). Such an imbalance and energy deficiency at the cell level compromise its ability to adapt to physiological stress to which it is exposed. This in fine contributes to the cell aging phenomenon (Trifunovic A. and al., J. of Internal Medicine, vol. 263, pp. 167-178). It is also admitted that these disruptions originating from mitochondria are clearly involved with the genesis of a large spectrum of pathologies or tissue disorders (Barlow-Stewart K., The Australasian Genetics Ressource Book, 2007, pp. 1-3 and quoted references).
Source of intracellular ROS, mitochondria remains the main target. Consequently and in order to preserve at best the functional and/or structural integrity of any mitochondria, one of the current concerns of many researchers is to reduce the oxidative metabolism originating from mitochondria and to stimulate or to protect the mitochondria functions.
In the state of the art displayed these last years with same objectives, retained strategies and systems are often shared among:                the selection of powerful antioxidants that carry one or several thiol or phenol moities, and that are found at the natural state in the animal or plant kingdoms, like thioctic acid better known as alpha-lipoic acid with evidenced benefits against the mitochondrial aging (Palaniappan A. R. and al., Neurochem. Res., 2007, vol. 32, pp. 1552-8), or else ergothionein that is a thiourea derivative announced to protect the mitochondria membranes of mammals (U.S. Pat. No. 6,479,533),        the use of some molecules or conventional antioxidant proteins, however modified by the addition/grafting of groups or sequences (hydrophobic cation, etc.) with a strong affinity for mitochondria and for a greater inner storage (Kagan V. E. and al., Adv. Drug Delivery Rev., 2009, vol. 61, pp. 1375-85),        the development of small peptides announced “cell-permeable” that alternate some basic and aromatic aminoacid residues, due to their ability to penetrate the mitochondrial inner membrane and then to express within it some properties of cyto- and mitoprotection (Szeto H. H., Antioxidants & Redox Signaling, 2008, vol. 3, pp. 1-15).        